The major aims of this proposal are three-fold: 1) to determine whether the colon is involved in the postprandial intestinal hyperemia, 2) to identify the constituents of bile which are responsible for the bile-induced ileal hyperemia, and 3) to assess the relative contributions of neural, humoral, and/or metabolic factors to the postprandial intestinal hyperemia. In conscious animals, the magnitude and time course of the postprandial intestinal hyperemia along the intestinal tract will be assessed with the radioactive microspere method. Particular emphasis will be placed on the involvement of the colon in the hyperemic response. Acute experimental models will be used to identify the constituents of chyme responsible for the hyperemia and to assess the mechanisms involved. Various constituents of chyme will be placed in the lumen of denervated in situ intestinal preparations (jejunum, ileum, and colon) and their effects on intestinal blood flow and oxygen uptake assessed. Particular emphasis will be placed on identifying the constituents of bile responsible for the bile-induced ileal hyperemia. The involvement of neural and humoral factors in the small intestinal hyperemia will be assessed by comparing the vascular effects of intralumenal placement of constituents of chyme (e.g. micellar oleic acid in the jejunum, bile in the ileum) before and after administration of humoral and neural antagonists. The role of metabolic factors will be evaluated by assessing the effects of the transported or metabolized constituents of chyme on intestinal hemodynamics and oxygenation; these observations will be compared to results acquired using the corresponding non-transported or non-metabolized analogues.